You need to get calories from somewhere, should it be from carbohydrate or fat?

Monday, June 23, 2008

Diabetes in Sweden update

Just an update from Nielson and Joensson, original comment here. Happened on it while chasing assorted lipoprotein numbers for another post.

HbA1c below 5% without meds is possible through diet. I wouldn't describe these people as cured, a pizza a week would have them in trouble, but with HbA1c this low I'd not be worrying about CVD too much.

"Of the total of 10 controls, who have switched diet, 2 persons after a weight reduction of 20 kg each are free of all signs of diabetes after 3 and 2 years respectively i.e. HbA1c below 5.0%, fasting blood glucose below 5.0 mmol/l and free of any blood glucose lowering medication"

Second comment is that, even with successful weight loss and diabetes imporvement, carb creep is real and hard to avoid.

I know that rye crisp bread was a feature of this diet. I wonder what would have happened in the complete absence of gluten? Or whether the problems of removing this potentially addictive carbohydrate source would just have sabotaged the initial compliance?

My HbA1C is never below 5... I've had it measured twice and the first time it was 5.4 and the second it was 5.1. In fact, the blood test when it came up 5.4, my fructosamine was 255, which implies a very high average 2 week blood sugar (fructosamine 255 = a1c 5.9!)

I'm thin and eat 60 carbs/day and I don't eat a lot of calories... I'm not diabetic. In fact, my a1c was worse when I was eating less calories and was underweight, presumably because glucose control was not as good as a result of the stress and low leptin (which would make sense, because I felt my blood sugar was all screwy and was always getting hypoglycemia back then, in spite of eating less calories and not more carbs).

Even when I was strict ketogenic dieting and eating low calorie (while actively losing weight) my fructosamine was 204, which translates into an a1c of about 5. This should have been the best possible glucose control - I was not underweight, I was actively losing weight, and I was eating ketogenic. Even then, my a1c was only 5.

I should also mention that I do have blood glucose abnormalities - I have extremely brittle sugar (very unstable) but am almost always fasting hypoglycemia, 59-69 range. Considering my experiences as a non-diabetic, I can't imagine how it is realistic for a diabetic to get their a1c under 5, and have that be worth it (i.e. not loading themselves up with excessive drugs or starving constantly).

The central problem in the most common form of Type 2 Diabetes mellitus and the Metabolic Syndrome is the infiltration of the islets of Langerhans in the pancreas with amyloid. This disrupts the islet architecture, causing the alpha cells to lose touch with their companion beta cells, which in turn has the effect of causing them to secrete glucagon inappropriately and in relatively large amounts regardless of the blood sugar level.

When glucagon is secreted in large quantities, regardless of the blood sugar level, the liver is stimulated to secrete inappropriate amounts of glucose into the blood of the resting person. This raises the blood sugar level, which stimulates the beta cells in the islets to secrete insulin

"Because of a certain kind of protein plaque in the pancreas, the person with diabete makes too much blood sugar-making hormone."

(Personally, I don't know if it is appropriate to view amyloidosis as the point of origin defect in hyperglycemia from the liver. It was my understanding that amyloidosis is a RESULT of hyperinsulinemia, because insulin degrading enzyme also prevents amyloidosis. If hyperinsulinemia already exists, that means glucose from the liver and diet is / was already abnormally regulated.)

http://www.jbc.org/cgi/content/abstract/277/16/13389

"When insulin, a well characterized substrate of IDE [insulin degrading enzyme], was added to the in vitro degradation assay, removal of AICD [a precursor to amyloid] was efficiently blocked."

The body probably uses cross talk between cells to control everything. The pancreas has beta cells which secrete insulin when glucose levels are too high. It also contains alpha cells which secrete glucagon when glucose levels are too low. The cells are right next door to each other. As well as both types of cell monitoring glucose it seems as if the glucagon secreting cells look at the local amount of insulin being secreted and use this as a signal to moderate their glucagon secretion. There is no point in trying to raise blood sugar levels with glucagon when the body is producing lots of insulin due to a recent meal intake. It's probably a fine tuning mechanism which can be over ridden by catastrophic changes in glucose. The beta amyloid is debris which blocks this fine tuning mechanism and results in over secretion of glucagon which raises blood glucose inappropriately.

This looks to be a failsafe mechanism. If you have a problem with your blood glucose control it's better high than low. An hour of hyperglycaemia is survivable. An hour with a glucose of 0.5mmol/l may not be. Fail to high glucose. Fail to diabetes rather than acute death... Hee hee, could the ADA be correct? Only joking!

Personally I feel it is probably a significant effect but not primary. Hyperglycaemic failure of the vagus nerve supply to the liver (and probably the pancreas too) may well have similar effects on blood glucose but are not primary.

These are probably reasons why LC side steps type 2 diabetes but doesn't cure. Also why it works well for most but not all.

Beta amyloid is also a feature (probably significant) of the damage in the brain in excitotoxin diseases (Parkinsons, ALS, Alzheimers) and I doubt very much whether it is primary there either.

About Me

I am Petro Dobromylskyj, always known as Peter. I'm a vet, trained at the RVC, London University. I was fortunate enough to intercalate a BSc degree in physiology in to my veterinary degree. I was even more fortunate to study under Patrick Wall at UCH, who set me on course to become a veterinary anaesthetist, mostly working on acute pain control. That led to the Certificate then Diploma in Veterinary Anaesthesia and enough publications to allow me to enter the European College of Veterinary Anaesthesia and Analgesia as a de facto founding member. Anaesthesia teaches you a lot. Basic science is combined with the occasional need to act rapidly. Wrong decisions can reward you with catastrophe in seconds. Thinking is mandatory.
I stumbled on to nutrition completely by accident. Once you have been taught to think, it's hard to stop. I think about lots of things. These are some of them.

Organisation (or lack of it)!

The "labels" function on this blog has been used to function as an index and I've tended to group similar subjects together by using labels starting with identical text. If they're numbered within a similar label, start with (1). The archive is predominantly to show the posts I've put up in the last month, if people want to keep track of recent goings on. I might change it to the previous week if I ever get to time to put up enough posts in a week to justify it. That seems to be the best I can do within the limits of this blogging software!